Results 101 to 110 of about 29,089 (240)
Proteostasis of organelles in aging and disease
Cells rely on regulated proteostasis mechanisms to keep their internal compartments functioning properly. When these mechanisms fail, damaged proteins accumulate, disrupting organelles, such as the nucleus, mitochondria, endoplasmic reticulum, Golgi, and lysosomes, as well as membraneless organelles, such as stress granules, processing bodies, the ...
Yara Nabawi +5 more
wiley +1 more source
Platelet activating factor (PAF) is an inflammatory phospholipid signaling molecule implicated in synaptic plasticity, learning and memory and neurotoxicity during neuroinflammation.
Jennetta W Hammond +2 more
doaj +1 more source
Variability in intracellular localization of D‐amino acid oxidase in choroid plexus epithelial cells
D‐amino acid oxidase (DAO) in choroid plexus epithelial cells (CPECs) shows vesicle‐like localization by histological and super‐resolution analyses. DAO colocalizes with peroxisomal, Golgi, endosomal, lysosomal, autophagosomal, and exosomal markers, indicating diverse subcellular distribution. This suggests DAO is transported within CPECs to metabolize
Koji Ono +3 more
wiley +1 more source
α-Synuclein: A Multifunctional Player in Exocytosis, Endocytosis, and Vesicle Recycling
α-synuclein (α-Syn) is a presynaptic enriched protein involved in the pathogenesis of Parkinson’s disease. However, the physiological roles of α-Syn remain poorly understood.
Mingzhu Huang +9 more
doaj +1 more source
Morphologic and functional correlates of synaptic pathology in the cathepsin D knockout mouse model of congenital neuronal ceroid lipofuscinosis [PDF]
Mutations in the cathepsin D (CTSD) gene cause an aggressive neurodegenerative disease (congenital neuronal ceroid lipofuscinosis) that leads to early death. Recent evidence suggests that presynaptic abnormalities play a major role in the pathogenesis of
Andrew Edwards +13 more
core +1 more source
Abstract Alzheimer's disease (AD) is neuropathologically defined by amyloid‐beta (Aβ) plaques and tau neurofibrillary tangles. However, co‐pathologies and other pathobiological processes are involved in the pathogenesis of AD, contributing to neurodegeneration and clinical symptoms.
Daniel Ferreira +9 more
wiley +1 more source
Intramuscular pathways of maladaptation in overtraining syndrome
Abstract figure legend The transition from adaptive overreaching to maladaptive overtraining and mechanisms through which excessive training load can lead to performance decline. Four interconnected pathophysiological domains are highlighted: neural fatigue, involving both central and peripheral components such as altered sensory feedback and reflex ...
Emily Shorter +4 more
wiley +1 more source
Abstract figure legend The capillary–mitochondria–ion channel (CMIC) axis scales structural resources to match functional workload. (Left) In settings of restricted energetic capacity (e.g. cortical neurons), sparse capillary networks and modest mitochondrial pools set a lower energetic ceiling, sufficient to support phasic, low‐workload excitability. (
L. Fernando Santana, Scott Earley
wiley +1 more source
ABSTRACT Aim The alkali cation/proton exchanger NHE6/SLC9A6 regulates luminal pH homeostasis and trafficking of recycling endosomes in most tissues, especially neurons. Loss‐of‐function mutations in NHE6 cause Christianson Syndrome, an X‐linked neurodevelopmental and neurodegenerative disorder; however, the underlying molecular and cellular mechanisms ...
Rebecca Flessner +6 more
wiley +1 more source
FM1-43 reveals membrane recycling in adult inner hair cells of the mammalian cochlea [PDF]
Neural transmission of complex sounds demands fast and sustained rates of synaptic release from the primary cochlear receptors, the inner hair cells (IHCs). The cells therefore require efficient membrane recycling.
Ashmore, JF +2 more
core +1 more source

